A Better Understanding of Menopause to Help You Intervene with Best Nursing Practices
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Androgen Excess in Breast Cancer Development: Implications for Prevention and Treatment
26 2 Endocrine-Related G Secreto et al. Androgen excess in breast 26:2 R81–R94 Cancer cancer development REVIEW Androgen excess in breast cancer development: implications for prevention and treatment Giorgio Secreto1, Alessandro Girombelli2 and Vittorio Krogh1 1Epidemiology and Prevention Unit, Fondazione IRCCS – Istituto Nazionale dei Tumori, Milano, Italy 2Anesthesia and Critical Care Medicine, ASST – Grande Ospedale Metropolitano Niguarda, Milano, Italy Correspondence should be addressed to G Secreto: [email protected] Abstract The aim of this review is to highlight the pivotal role of androgen excess in the Key Words development of breast cancer. Available evidence suggests that testosterone f breast cancer controls breast epithelial growth through a balanced interaction between its two f ER-positive active metabolites: cell proliferation is promoted by estradiol while it is inhibited by f ER-negative dihydrotestosterone. A chronic overproduction of testosterone (e.g. ovarian stromal f androgen/estrogen balance hyperplasia) results in an increased estrogen production and cell proliferation that f androgen excess are no longer counterbalanced by dihydrotestosterone. This shift in the androgen/ f testosterone estrogen balance partakes in the genesis of ER-positive tumors. The mammary gland f estradiol is a modified apocrine gland, a fact rarely considered in breast carcinogenesis. When f dihydrotestosterone stimulated by androgens, apocrine cells synthesize epidermal growth factor (EGF) that triggers the ErbB family receptors. These include the EGF receptor and the human epithelial growth factor 2, both well known for stimulating cellular proliferation. As a result, an excessive production of androgens is capable of directly stimulating growth in apocrine and apocrine-like tumors, a subset of ER-negative/AR-positive tumors. -
Estrogen Deficiency During Menopause and Its Management: a Current Update V
Review Article Estrogen deficiency during menopause and its management: A current update V. T. Hemalatha1, A. Julius2, S. P. Kishore Kumar3, L. Vijayalakshmi4, Shankar Narayanan1 ABSTRACT Different phases of a woman’s life: Puberty, menses, pregnancy, and menopause have varied influence on her oral health. During the menopause, women go through biological and endocrine changes, particularly in their sex steroid hormone production, affecting their health. Sex hormones strongly influence body fat distribution and adipocyte differentiation. Estrogens and testosterone differentially affect adipocyte physiology, but the importance of estrogens in the development of metabolic diseases during menopause is disputed. Estrogens and estrogens receptor regulate various aspects of glucose and lipid metabolism. Disturbances of this metabolic signal lead to the development of metabolic syndrome and a higher cardiovascular risk in woman. The absence of estrogens is a clue factor in the onset of cardiovascular disease during the menopausal period, which is characterized by lipid profile variations and predominant abdominal fat accumulation. However, influence of the absence of these hormones and its relationship to higher obesity in women during menopause is not clear. This systematic review discusses of the role of estrogens and estrogen receptors in adipocyte differentiation and its various effects and brief discussion on its management. KEY WORDS: Estrogen hormone (estrogens/progestogens) replacement therapy, Menopause, Weight gain INTRODUCTION BODY CHANGES AT MENOPAUSE Menopause occurs when a woman stops ovulating and As we age, our muscles decrease in bulk and our her monthly period (menstruation) stops. metabolism slows down. These changes cancontribute to weight gain around the time of menopause. Other As women age, into their 40s and 50s, there is a tendency physical changes associated with menopause may to gain weight. -
Diverse Pathomechanisms Leading to the Breakdown of Cellular Estrogen Surveillance and Breast Cancer Development: New Therapeutic Strategies
Journal name: Drug Design, Development and Therapy Article Designation: Review Year: 2014 Volume: 8 Drug Design, Development and Therapy Dovepress Running head verso: Suba Running head recto: Diverse pathomechanisms leading to breast cancer development open access to scientific and medical research DOI: http://dx.doi.org/10.2147/DDDT.S70570 Open Access Full Text Article REVIEW Diverse pathomechanisms leading to the breakdown of cellular estrogen surveillance and breast cancer development: new therapeutic strategies Zsuzsanna Suba Abstract: Recognition of the two main pathologic mechanisms equally leading to breast cancer National Institute of Oncology, development may provide explanations for the apparently controversial results obtained by sexual Budapest, Hungary hormone measurements in breast cancer cases. Either insulin resistance or estrogen receptor (ER) defect is the initiator of pathologic processes and both of them may lead to breast cancer development. Primary insulin resistance induces hyperandrogenism and estrogen deficiency, but during these ongoing pathologic processes, ER defect also develops. Conversely, when estrogen resistance is the onset of hormonal and metabolic disturbances, initial counteraction is For personal use only. hyperestrogenism. Compensatory mechanisms improve the damaged reactivity of ERs; however, their failure leads to secondary insulin resistance. The final stage of both pathologic pathways is the breakdown of estrogen surveillance, leading to breast cancer development. Among pre- menopausal breast cancer cases, insulin resistance is the preponderant initiator of alterations with hyperandrogenism, which is reflected by the majority of studies suggesting a causal role of hyperandrogenism in breast cancer development. In the majority of postmenopausal cases, tumor development may also be initiated by insulin resistance, while hyperandrogenism is typi- cally coupled with elevated estrogen levels within the low postmenopausal hormone range. -
Management of Women with Premature Ovarian Insufficiency
Management of women with premature ovarian insufficiency Guideline of the European Society of Human Reproduction and Embryology POI Guideline Development Group December 2015 1 Disclaimer The European Society of Human Reproduction and Embryology (hereinafter referred to as 'ESHRE') developed the current clinical practice guideline, to provide clinical recommendations to improve the quality of healthcare delivery within the European field of human reproduction and embryology. This guideline represents the views of ESHRE, which were achieved after careful consideration of the scientific evidence available at the time of preparation. In the absence of scientific evidence on certain aspects, a consensus between the relevant ESHRE stakeholders has been obtained. The aim of clinical practice guidelines is to aid healthcare professionals in everyday clinical decisions about appropriate and effective care of their patients. However, adherence to these clinical practice guidelines does not guarantee a successful or specific outcome, nor does it establish a standard of care. Clinical practice guidelines do not override the healthcare professional's clinical judgment in diagnosis and treatment of particular patients. Ultimately, healthcare professionals must make their own clinical decisions on a case-by-case basis, using their clinical judgment, knowledge, and expertise, and taking into account the condition, circumstances, and wishes of the individual patient, in consultation with that patient and/or the guardian or carer. ESHRE makes no warranty, express or implied, regarding the clinical practice guidelines and specifically excludes any warranties of merchantability and fitness for a particular use or purpose. ESHRE shall not be liable for direct, indirect, special, incidental, or consequential damages related to the use of the information contained herein. -
A Pharmaceutical Product for Hormone Replacement Therapy Comprising Tibolone Or a Derivative Thereof and Estradiol Or a Derivative Thereof
Europäisches Patentamt *EP001522306A1* (19) European Patent Office Office européen des brevets (11) EP 1 522 306 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.7: A61K 31/567, A61K 31/565, 13.04.2005 Bulletin 2005/15 A61P 15/12 (21) Application number: 03103726.0 (22) Date of filing: 08.10.2003 (84) Designated Contracting States: • Perez, Francisco AT BE BG CH CY CZ DE DK EE ES FI FR GB GR 08970 Sant Joan Despi (Barcelona) (ES) HU IE IT LI LU MC NL PT RO SE SI SK TR • Banado M., Carlos Designated Extension States: 28033 Madrid (ES) AL LT LV MK (74) Representative: Markvardsen, Peter et al (71) Applicant: Liconsa, Liberacion Controlada de Markvardsen Patents, Sustancias Activas, S.A. Patent Department, 08028 Barcelona (ES) P.O. Box 114, Favrholmvaenget 40 (72) Inventors: 3400 Hilleroed (DK) • Palacios, Santiago 28001 Madrid (ES) (54) A pharmaceutical product for hormone replacement therapy comprising tibolone or a derivative thereof and estradiol or a derivative thereof (57) A pharmaceutical product comprising an effec- arate or sequential use in a method for hormone re- tive amount of tibolone or derivative thereof, an effective placement therapy or prevention of hypoestrogenism amount of estradiol or derivative thereof and a pharma- associated clinical symptoms in a human person, in par- ceutically acceptable carrier, wherein the product is pro- ticular wherein the human is a postmenopausal woman. vided as a combined preparation for simultaneous, sep- EP 1 522 306 A1 Printed by Jouve, 75001 PARIS (FR) 1 EP 1 522 306 A1 2 Description [0008] The review article of Journal of Steroid Bio- chemistry and Molecular Biology (2001), 76(1-5), FIELD OF THE INVENTION: 231-238 provides a review of some of these compara- tive studies. -
Virilization and Enlarged Ovaries in a Postmenopausal Woman
Please do not remove this page Virilization and Enlarged Ovaries in a Postmenopausal Woman Guerrero, Jessenia; Marcus, Jenna Z.; Heller, Debra https://scholarship.libraries.rutgers.edu/discovery/delivery/01RUT_INST:ResearchRepository/12643454200004646?l#13643490680004646 Guerrero, J., Marcus, J. Z., & Heller, D. (2017). Virilization and Enlarged Ovaries in a Postmenopausal Woman. In International Journal of Surgical Pathology (Vol. 25, Issue 6, pp. 507–508). Rutgers University. https://doi.org/10.7282/T3125WCP This work is protected by copyright. You are free to use this resource, with proper attribution, for research and educational purposes. Other uses, such as reproduction or publication, may require the permission of the copyright holder. Downloaded On 2021/09/25 21:27:45 -0400 Virilization and Enlarged Ovaries in a Postmenopausal Woman Abstract: A patient with postmenopausal bleeding and virilization was found to have bilaterally enlarged ovaries with a yellow cut surface. Histology revealed cortical stromal hyperplasia with stromal hyperthecosis. This hyperplastic condition should not be mistaken for an ovarian neoplasm. Key words: Ovary, ovarian neoplasms, virilization Introduction Postmenopausal women who present with clinical manifestations of hyperandrogenism are often presumed to have an androgen-secreting tumor, particularly if there is ovarian enlargement. Gross findings in the ovaries can help exclude an androgen-secreting ovarian tumor and histologic findings can confirm the gross findings. Case A 64 year old woman with abnormal hair growth, male pattern baldness, clitorimegaly and postmenopausal bleeding presented to the clinic for evaluation of a possible hormone secreting tumor. Pre-operative work-up revealed bilateral ovarian enlargement, measuring 4 cm in greatest dimension, without evidence of an ovarian or adrenal tumor. -
A Novel Null Mutation in P450 Aromatase Gene (CYP19A1
J Clin Res Pediatr Endocrinol 2016;8(2):205-210 DO I: 10.4274/jcrpe.2761 Ori gi nal Ar tic le A Novel Null Mutation in P450 Aromatase Gene (CYP19A1) Associated with Development of Hypoplastic Ovaries in Humans Sema Akçurin1, Doğa Türkkahraman2, Woo-Young Kim3, Erdem Durmaz4, Jae-Gook Shin3, Su-Jun Lee3 1Akdeniz University Faculty of Medicine Hospital, Department of Pediatric Endocrinology, Antalya, Turkey 2Antalya Training and Research Hospital, Clinic of Pediatric Endocrinology, Antalya, Turkey 3 Inje University College of Medicine, Department of Pharmacology, Inje University, Busan, Korea 4İzmir University Faculty of Medicine, Medical Park Hospital, Clinic of Pediatric Endocrinology, İzmir, Turkey ABS TRACT Objective: The CYP19A1 gene product aromatase is responsible for estrogen synthesis and androgen/estrogen equilibrium in many tissues, particularly in the placenta and gonads. Aromatase deficiency can cause various clinical phenotypes resulting from excessive androgen accumulation and insufficient estrogen synthesis during the pre- and postnatal periods. In this study, our aim was to determine the clinical characteristics and CYP19A1 mutations in three patients from a large Turkish pedigree. Methods: The cases were the newborns referred to our clinic for clitoromegaly and labial fusion. Virilizing signs such as severe acne formation, voice deepening, and clitoromegaly were noted in the mothers during pregnancy. Preliminary diagnosis was aromatase deficiency. Therefore, direct DNA sequencing of CYP19A1 was performed in samples from parents (n=5) and patients (n=3). WHAT IS ALREADY KNOWN ON THIS TOPIC? Results: In all patients, a novel homozygous insertion mutation in the fifth exon (568insC) was found to cause a frameshift in the open reading frame and to truncate Aromatase deficiency can cause various clinical phenotypes the protein prior to the heme-binding region which is crucial for enzymatic activity. -
Spanish Consensus on Premature Menopause
Maturitas 80 (2015) 220–225 Contents lists available at ScienceDirect Maturitas jou rnal homepage: www.elsevier.com/locate/maturitas Spanish consensus on premature menopause a,∗ a b c d Nicolás Mendoza , M Dolores Juliá , Daniela Galliano , Pluvio Coronado , e f f g h Begona˜ Díaz , Juan Fontes , José Luis Gallo , Ana García , Misericordia Guinot , i j k j l Merixtell Munnamy , Beatriz Roca , Manuel Sosa , Jordi Tomás , Plácido Llaneza , m Rafael Sánchez-Borrego a University of Granada, Obstetric and Gynecologic, Granada, Spain b Hospital Universitario la Fe de Valencia, Spain c Instituto Valenciano de Infertilidad (IVI), Barcelona, Spain d University of Madrid (Complutense), Obstetric and Gynecologic, Hospital Clínico San Carlos, Madrid, Spain e Complejo Hospitalario Universitario de Albacete, Spain f Hospital Virgen de las Nieves de Granada, Spain g Instituto Valenciano de Oncología, Spain h Hospital Clinic Barcelona, Spain i Sant Feliu de Llobregat, Barcelona, Spain j Hospital Universitari Mutua Terrassa, Spain k Hospital Materno-Infantil de Canarias, Spain l University of Oviedo, Obstetric and Gynecologic, Hospital Central de Asturias, Spain m Clínica Diatros, Barcelona, Spain a r t i c l e i n f o a b s t r a c t Article history: Introduction: While we recognise that the term premature menopause is more accepted by most non- Received 18 September 2014 specialist health care providers and by the general population, ‘primary ovarian insufficiency’ (POI) is Received in revised form 3 November 2014 currently considered the most apposite term to explain the loss of ovarian function, because it better Accepted 12 November 2014 explains the variability of the clinical picture, does not specify definitive failure, and highlights the specific ovarian source. -
Functional Hypothalamic Amenorrhea: a Stress-Based Disease
Review Functional Hypothalamic Amenorrhea: A Stress-Based Disease Agnieszka Podfigurna and Blazej Meczekalski * Department of Gynecological Endocrinology, Poznan University of Medical Sciences, 60-701 Poznan, Poland; agnieszkapodfi[email protected] * Correspondence: [email protected]; Tel.: +0048-6184-1933 Abstract: The aim of the study is to present the problem of functional hypothalamic amenorrhea, taking into account any disease and treatment, diagnosis, and consequences of this disease. We searched PubMed (MEDLINE) and included 38 original and review articles concerning functional hypothalamic amenorrhea. Functional hypothalamic amenorrhea is the most common cause of secondary amenorrhea in women of childbearing age. It is a reversible disorder caused by stress related to weight loss, excessive exercise and/or traumatic mental experiences. The basis of functional hypothalamic amenorrhea is hormonal, based on impaired pulsatile GnRH secretion in the hypotha- lamus, then decreased secretion of gonadotropins, and, consequently, impaired hormonal function of the ovaries. This disorder leads to hypoestrogenism, manifested by a disturbance of the menstrual cycle in the form of amenorrhea, leading to anovulation. Prolonged state of hypoestrogenism can be very detrimental to general health, leading to many harmful short- and long-term consequences. Treatment of functional hypothalamic amenorrhea should be started as soon as possible, and it should primarily involve lifestyle modification. Only then should pharmacological treatment be applied. Importantly, treatment is most often long-term, but it results in recovery for the majority of patients. Effective therapy, based on multidirectional action, can protect patients from numerous negative impacts on fertility, cardiovascular system and bone health, as well as reducing mental morbidity. Citation: Podfigurna, A.; Meczekalski, B. -
Hyperestrogenism
Hyperestrogenism (Estrogen Toxicity) Basics OVERVIEW • “Hyperestrogenism” refers to a condition in which excessive estrogen is present in the body • A syndrome characterized by high serum concentration of estrogens (estradiol, estriol, or estrone) • Estrogens are hormones that are produced by the female (ovary, placenta), male (testicles), by both sexes (adrenal glands), and by some plants; most commonly recognized as a female sex hormone that is responsible for normal sexual behavior and development and function of the female reproductive tract; in the male, estrogens are responsible for Leydig cell function, which produce testosterone • Hyperestrogenism may occur as a result of excessive estrogen secretion in the body or administration of estrogen-containing medications, such as diethylstilbestrol or estriol SIGNALMENT/DESCRIPTION OF PET Species • Dogs Mean Age and Range • Older female dogs (secondary to tumors of the ovaries; follicular ovarian cysts, in which the area containing the egg [known as the “follicle”] in the ovary develops, but ovulation does not occur normally) • Young female dogs (secondary to follicular ovarian cysts) • Older male dogs (secondary to tumors of the testicles) • If from exposure to estrogenic medications, all ages, breeds, genders; toy breed exposure to owner transdermal hormone replacement therapy patches SIGNS/OBSERVED CHANGES IN THE PET • Attractive to intact male dogs (intact male dogs are capable of reproducing) • Infertility • Prolonged heat (specifically proestrus and estrus) in females • Decreased -
Diagnosis and Management of Primary Amenorrhea and Female Delayed Puberty
6 184 S Seppä and others Primary amenorrhea 184:6 R225–R242 Review MANAGEMENT OF ENDOCRINE DISEASE Diagnosis and management of primary amenorrhea and female delayed puberty Satu Seppä1,2 , Tanja Kuiri-Hänninen 1, Elina Holopainen3 and Raimo Voutilainen 1 Correspondence 1Departments of Pediatrics, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland, should be addressed 2Department of Pediatrics, Kymenlaakso Central Hospital, Kotka, Finland, and 3Department of Obstetrics and to R Voutilainen Gynecology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland Email [email protected] Abstract Puberty is the period of transition from childhood to adulthood characterized by the attainment of adult height and body composition, accrual of bone strength and the acquisition of secondary sexual characteristics, psychosocial maturation and reproductive capacity. In girls, menarche is a late marker of puberty. Primary amenorrhea is defined as the absence of menarche in ≥ 15-year-old females with developed secondary sexual characteristics and normal growth or in ≥13-year-old females without signs of pubertal development. Furthermore, evaluation for primary amenorrhea should be considered in the absence of menarche 3 years after thelarche (start of breast development) or 5 years after thelarche, if that occurred before the age of 10 years. A variety of disorders in the hypothalamus– pituitary–ovarian axis can lead to primary amenorrhea with delayed, arrested or normal pubertal development. Etiologies can be categorized as hypothalamic or pituitary disorders causing hypogonadotropic hypogonadism, gonadal disorders causing hypergonadotropic hypogonadism, disorders of other endocrine glands, and congenital utero–vaginal anomalies. This article gives a comprehensive review of the etiologies, diagnostics and management of primary amenorrhea from the perspective of pediatric endocrinologists and gynecologists. -
Steroidal Estrogens
FINAL Report on Carcinogens Background Document for Steroidal Estrogens December 13 - 14, 2000 Meeting of the NTP Board of Scientific Counselors Report on Carcinogens Subcommittee Prepared for the: U.S. Department of Health and Human Services Public Health Service National Toxicology Program Research Triangle Park, NC 27709 Prepared by: Technology Planning and Management Corporation Canterbury Hall, Suite 310 4815 Emperor Blvd Durham, NC 27703 Contract Number N01-ES-85421 Dec. 2000 RoC Background Document for Steroidal Estrogens Do not quote or cite Criteria for Listing Agents, Substances or Mixtures in the Report on Carcinogens U.S. Department of Health and Human Services National Toxicology Program Known to be Human Carcinogens: There is sufficient evidence of carcinogenicity from studies in humans, which indicates a causal relationship between exposure to the agent, substance or mixture and human cancer. Reasonably Anticipated to be Human Carcinogens: There is limited evidence of carcinogenicity from studies in humans which indicates that causal interpretation is credible but that alternative explanations such as chance, bias or confounding factors could not adequately be excluded; or There is sufficient evidence of carcinogenicity from studies in experimental animals which indicates there is an increased incidence of malignant and/or a combination of malignant and benign tumors: (1) in multiple species, or at multiple tissue sites, or (2) by multiple routes of exposure, or (3) to an unusual degree with regard to incidence, site or type of tumor or age at onset; or There is less than sufficient evidence of carcinogenicity in humans or laboratory animals, however; the agent, substance or mixture belongs to a well defined, structurally-related class of substances whose members are listed in a previous Report on Carcinogens as either a known to be human carcinogen, or reasonably anticipated to be human carcinogen or there is convincing relevant information that the agent acts through mechanisms indicating it would likely cause cancer in humans.